Molecular immunology · 2025
Plasma secretory protein genes in hepatocellular carcinoma and heart failure: Comorbidity and biological function exploration.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Cao Lizhi, Wang Xiaoying, Ning Zhongping, Xie Fandi, Li Xiaodan, Chen Yongting, Geng Qian, Liu Junchi, Zhu Qian, Ma Linlin, Li Yanfei
Аннотация
BACKGROUND: This research aimed to elucidate the roles of plasma secretory protein genes in mediating the comorbid effects between hepatocellular carcinoma (HCC) and heart failure (HF).
METHODS: A comprehensive analysis utilizing Weighted Gene Co-expression Network Analysis (WGCNA), differential expression analysis, and advanced deep learning techniques was conducted to identify three plasma-secreted protein genes (Ficolin-3: FCN3, Fibroblast Activation Protein: FAP, High Mobility Group Box 2: HMGB2) as key players in the comorbid interplay between HCC and HF.
RESULTS: Validation experiments confirmed the significant biological functions of these genes in disease pathogenesis. Additionally, dexamethasone and catechins were identified as promising candidates for pharmacological intervention in the prevention of HCC and HF.
CONCLUSION: These findings unveil potential mechanistic pathways of comorbidity between HCC and HF, providing novel biological markers and therapeutic targets for the prognostic evaluation and treatment of these conditions, with substantial implications for refining clinical diagnosis and therapeutic strategies.
METHODS: A comprehensive analysis utilizing Weighted Gene Co-expression Network Analysis (WGCNA), differential expression analysis, and advanced deep learning techniques was conducted to identify three plasma-secreted protein genes (Ficolin-3: FCN3, Fibroblast Activation Protein: FAP, High Mobility Group Box 2: HMGB2) as key players in the comorbid interplay between HCC and HF.
RESULTS: Validation experiments confirmed the significant biological functions of these genes in disease pathogenesis. Additionally, dexamethasone and catechins were identified as promising candidates for pharmacological intervention in the prevention of HCC and HF.
CONCLUSION: These findings unveil potential mechanistic pathways of comorbidity between HCC and HF, providing novel biological markers and therapeutic targets for the prognostic evaluation and treatment of these conditions, with substantial implications for refining clinical diagnosis and therapeutic strategies.